These studies have focused on the pathogenic processes of experimental autoimmune uveitis (EAU). This intraocular inflammatory disease is induced by immunization with a retinal protein, S-antigen, and is considered a model for certain human uveitic conditions. Noteworthy findings: (1) A large portion of rats with EAU were found to develop pathological changes in the pineal gland. This finding supports the notion that the pineal gland of the mammals retains certain features of its being the "third eye." (2) As shown previously, EAU may be adoptively transferred from affected rats to naive recipients by sensitized lymphocytes which are injected systemically. However, no pathological changes were found following the injection of the active lymphocytes into the vitreous. This finding is interpreted to suggest that the lymphocytes undergo certain systemic processes which occur before the lymphocytes gain the capacity to induce EAU. (3) The genetic control of the capacity to develop EAU was further established with rats of the LeR strain. Unlike rats of the susceptible original strain (Lewis), LeR rats failed to develop EAU when immunized with S-antigen by the conventional way. However, EAU was induced when LeR rats were also injected with the Bordetella pertussis bacteria. These bacteria enhance the immediate hypersensitivity system, and the hypothesis that LeR rats are deficient in this system has been further supported by the findings that LeR rats do not develop normal immediate hypersensitivity skin responses and have markedly reduced numbers of mast cells in their choroid (about 1/5 of the number found in the matched Lewis rats). These findings show that immediate hypersensitivity and the mast cell system play an important role in the development of EAU, presumably by increasing the permeability of the retinal blood vesels.